Article written by
Dr. Neha Rai
MBBS, MD SR AIIMS Patna
Diabetes Mellitus refers to a group of common metabolic disorders that share the phenotype of hyperglycaemia and are caused by a complex interaction of genetics and environmental factors. It is very different from Diabetes Insipidus. Diabetes Insipidus is a syndrome characterised by the production of abnormally large volumes of dilute urine due to decreased secretion or action of Vasopressin, a hormone secreted by the posterior pituitary gland.
The pathogenic process leading to hyperglycaemia is the basis for classification of diabetes mellitus into several types. Age or insulin dependence are no longer the criteria for differentiation. Type I and Type II are the two broad categories. In Type I DM there is destruction of pancreatic β cells and insulin deficiency resulting from autoimmune β cell destruction. Type II DM is characterised by variable degree of insulin resistance, impaired insulin secretion, excessive hepatic glucose production and abnormal fat metabolism.
Glucose homeostasis reflects balance between hepatic glucose production and peripheral glucose uptake & utilization under the influence of various hormones like insulin, glucagon, cortisol, epinephrine etc. Normal fasting plasma glucose (FPG) level is <100mg/dl & 2-hour plasma glucose level is <140 mg/dl. In DM FPG is ≥126 mg/dl & 2-hr PG ≥200 mg/dl. FPG 100-125 mg/dl & 2-hr PG 140-199 mg/dl is termed as pre-diabetes.
Metabolic Derangements in Diabetes Mellitus
1. Carbohydrate Metabolism
Insulin deficiency or resistance impairs glucose uptake, less activation of insulin dependent enzymes leading to inhibition of glycolysis and stimulation of gluconeogenesis in the liver which contribute to hyperglycaemia.
2. Lipid Metabolism
Impaired fatty acid oxidation & lipid accumulation in skeletal muscle may generate reactive oxygen species (ROS) like lipid peroxides. Free fatty acid (FFA) flux from adipocytes is increased leading to increased lipid synthesis in hepatocytes which may lead to Fatty liver and dyslipidaemia.
3. Protein Metabolism
Increase breakdown of protein & amino acid for providing substrate for gluconeogenesis.
Clinical Presentation of Diabetes Mellitus
The person may present with cardinal symptoms of polyuria, polyphagia, polydipsia, glycosuria & weight loss. Patients often present with complaints of chronic recurrent infections.
Complications of Diabetes Mellitus
Acute metabolic complications of diabetes mellitus are diabetic ketoacidosis and hyperglycaemic hyperosmolar state.
Most common chronic metabolic complications of diabetes mellitus are retinopathy, neuropathy & nephropathy. Renal vascular microaneurysm, blot haemorrhage, and cotton wool spots are hallmarks of non-proliferative diabetic retinopathy whereas neovascularisation in response to retinal hypoxia is of proliferative diabetic retinopathy.
Distal symmetric polyneuropathy presenting with distal sensory loss is the most common form of diabetic neuropathy. Production of advanced glycation end products & diversion of glucose to sorbitol pathway are the proposed cause.
Persistent hyperglycaemia leading to glycation of basement membrane proteins may be the cause of nephropathy. Diabetic nephropathy may lead to chronic kidney disease. Chronic kidney disease (CKD) may lead to adynamic bone disease characterised by reduced bone volume & mineralization.
Hyperglycaemia helps colonization & growth of organisms along with abnormalities in cell mediated immunity and phagocyte function and diminished vascularisation leads to frequent infections like pneumonia, urinary tract infections, skin & soft tissue infections & periodontal diseases.
Oral Implications of Diabetes Mellitus
Following are the effects of DM in oral cavity:
- Increase gingivitis and periodontitis
- Increased caries incidence
- Delayed wound Healing
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| Fig 1. Factors responsible for Diabetic Wounds [1] |
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